We have isolated a substance from blood plasma which causes coronary vasoconstriction, augments the autoregulatory response, increases prostaglandin synthesis, in perfused rabbit hearts. Furthermore, this substance stimulates prostaglandin synthesis and counteracts indomethacin-induced inhibition in particulate enzyme preparations of both cardiac and renal tissues. In experiments outlined herein, we show that the action of the purified substance is unlike that of other substances which stimulate prostaglandin synthesis. Furthermore, the blood component stimulates synthesis of prostaglandin F2alpha at the expense of prostaglandins E2 and D2, but does not act in the same manner as other substances which favor synthesis of prostaglandin F. Our hypothesis is that (1) the physiological effects produced by this substance result from its effects on prostaglandin synthesis and thus (2) this substance should be effective in other systems involving prostaglandins and thromboxanes. In preliminary experiments, we found that the isolated blood component inhibits platelet aggregation, and also inhibits platelet thromboxane synthesis. These results support both parts of our hypothesis. We plan to further test this hypothesis by (1) investigating the causal relationships between inhibition of platelet aggregation and inhibition of platelet thromboxane synthesis produced by the blood component, (2) elucidating the mode of action of the blood component in prostaglandin, prostacyclin, and thromboxane synthesis in enzyme preparations, (3) comparing the physiological and biochemical effects of the blood component in organs or tissues which produce prostaglandins D, E and F with its effect systems that primarily synthesize thromboxanes or prostacyclin, and (4) examining the physiological or pathological conditions wherein the blood component plays a significant role.